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PubMed1966

[Acrodynia].

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Acrodynia↗
PubMed1984

[Morvan's fibrillary chorea and acrodynic syndrome following mercury treatment].

A 31 year-old inhabitant of French Guiana was prescribed mercuric iodide per os for two and a half months. Shortly before the end of the treatment he developed fasciculations in the trunk and particularly the lower limb muscles, distal painful paresthesias with vasomotor disorders, episodes of excessive perspiration and palmoplantar erythema, moderate fluctuating hypertension, progressive loss of weight and irritability with insomnia. Clinical and electrical signs of neuropathy were lacking. The clinical picture was that of Morvan's fibrillary chorea with acrodynia, the conditions of onset strongly suggesting a mercurial intoxication. Blood and particularly urine mercury levels were elevated. Administration of dimercaprol (BAL) considerably increased urinary excretion of mercury and there was progressive improvement and finally recovery after two months of BAL treatment. This case exemplifies the possible co-existence of fibrillary chorea and acrodynia. Whereas in many cases of fibrillary chorea a precise etiology cannot be determined, the affection can be induced by mercury as by gold administration. The fact that cases of fibrillary chorea due to mercury poisoning are rarely reported may be the result of individual patient hypersensitivity or particular metabolic absorption and excretion features of mercury. This case cannot be included within the continuous activity syndrome of muscle fibers described by Isaacs, since muscle contractures were absent and there was associated acrodynia. Moreover, there was no latent polyneuropathy, in spite of the intense fasciculations. It must be concluded, therefore, that in spite of its rarity fibrillary chorea should keep its semiologic autonomy.

Acrodynia↗
PubMed1995

[Arterial hypertension due to mercury poisoning: diagnostic value of captopril].

BACKGROUND: Mercury poisoning is a rare cause of hypertension in children. Urinary excretion sometimes remains low despite severe clinical intoxication. CASE REPORT: A 32 month-old girl was admitted with hypertension, tachycardia, apathy, irritability and excessive sweating. Erythromelalgia and neurologic symptoms permitted the diagnosis of acrodynia. Urine mercury remained normal until chelation. Captopril significantly increased urine mercury concentration but failed to improve clinical manifestations. Clinical improvement required infusions of BAL for 5 days then oral dimercaptosuccinic acid for 3 months. Metal vapors originated from the mercury which spilled from a broken thermometer onto the carpet. COMMENTS: Low basal urine mercury could be associated with real mercury poisoning. Small amounts of metal mercury held in a thermometer could produce a high level of mercury vapor leading to intoxication in young children. The binding capacity of metal ions by captopril could be used to increase urine mercury output. Nevertheless, captopril therapy fails to improve acrodynia. Total elimination of mercury requires long-term therapy with BAL or dimercaptosuccinic acid. CONCLUSIONS: An unexpected mode of intoxication and low basal urine mercury are not decisive arguments against mercury poisoning, which is the only cause of acrodynia.

Administration, Oral↗
PubMed1989

Pyridoxine deficiency and antagonism produce increased ground substance viscosity with resulting seborrheic dermatitis and increased tumor resistance.

Pyridoxine deficiency and 4'-deoxypyridoxine produce acrodynia in rats and seborrheic dermatitis in man. They also produce tumor inhibition in man and animals. Pyridoxine is extensively involved in metabolism and its relationship to the inhibitor 4'-deoxypyridoxine is complex. Pyridoxine deficiency and antagonism increases ground substance viscosity. This increase the inflammatory reactivity of the skin to produce acrodynia in rats and seborrheic dermatitis in man. The increase in ground substance viscosity would explain the increased resistance to tumors in man and animals. Pyridoxine is important in protein metabolism. The protein moiety of glycosaminoglycans in ground substance is small but plays a major role in tissue viscosity. Pyridoxine deficiency or antagonism by itself does not offer a definitive answer for tumors. Combined with substances that stimulate fibroblast or glycosaminoglycans production it may have a significant additive effect.

Acrodynia↗
PubMed1991

[Feer's disease].

Two sisters and their brother who had been exposed to mercury vapours from a broken fever thermometer were treated for acrodynia. Their urinary Hg concentrations, as well as the relatively few data that can be found in previous publications, show that the brain of children below the age of 5 years is much more sensitive to chronic mercury intoxication than the cerebrum of adults. Hg concentrations of well below 50 micrograms/l in the urine can be associated with severe symptoms. One of our patients had a mercury concentration of 6.3 micrograms/l. In adults with occupational exposure, urinary mercury concentrations of up to 200 micrograms/l are tolerated and permitted. Acrodynia possibly is not always diagnosed when it is occurring. Normal values for urinary Hg excretion in children under basal conditions and after administration of a chelating agent should be established.

Acrodynia↗
PubMed1984

Domestic metallic mercury poisoning.

In a family exposed to metallic mercury vapour two patients had acrodynia, one had the nephrotic syndrome, and one person remained well. Recognition of the variable manifestations of the disease and prevention of further exposure were the most important aspects of management. Recovery appeared to be complete as blood mercury levels fell to normal. Urinary mercury levels were too variable to be reliable as indications of progress.

Accidents, Home↗
PubMed2006

A Child with elemental mercury poisoning and unusual brain MRI findings.

Mercury vapor poisoning is a serious and potentially fatal problem. Neurological manifestations involving the central nervous system are seen with chronic mercury intoxication. We present the case of a 10-year-old child who demonstrated acrodynia, seizures, and visual impairment following 20 days of exposure to elemental mercury at home. The initial blood mercury concentration was 27.7 microg/L (normal <2 microg/L) and the initial 24-hour urine mercury concentration was 34.4 microg/L (normal =10 microg/L). After 9 months of treatment with D-penicillamine, the patient's clinical condition, biochemical laboratory parameters, and mercury concentrations all returned to normal. The T2-weighted MRI images of the patient's brain initially showed multiple hyperintense lesions in cerebral white matter, left globus pallidus, and putamen, which also improved.

Acrodynia↗
PubMed1997

The rise and fall of pink disease.

This paper explores the social and medical history and context of pink disease (acrodynia), a serious disease of infants and young children that baffled the medical world during the first half of the twentieth century until it was shown to be caused by mercury poisoning. In the English-speaking world the commonest source of the mercury was teething powders, which were widely available and advertised with increasing sophistication. Efforts to control them (such as the BMJ's campaign against 'Secret Remedies') were as yet unsuccessful. The article discusses the social conditions that influenced the existence and recognition of pink disease, the delay in finding its cause, the way in which it was explained as a virus infection or nutritional deficiency and why it seldom occurred outside the teething period. It discusses both professional and lay attitudes to health and diseases during the early twentieth century and provides a model of how the disease developed in a specific social setting and how the medical profession attempted to deal with it within the limitations of contemporary professional thought. The resistance to the evidence of mercury poisoning is typical of resistance to new medical knowledge and declined only when the opponents and sceptics grew old and disappeared from the scene. Meanwhile, the cause having been identified and accepted, pink disease disappeared, but its consequences emerged much later, in an unexpected quarter, as a cause of male infertility.

Acrodynia↗